1. During open heart surgery, the heart is arrested and protected by h
yperkalaemic cardioplegia. The coronary endothelium may be damaged by
ischaemia-reperfusion and cardioplegia. Subsequently, this may affect
cardiac function immediately after cardiac surgery and cause mortality
or morbidity. 2. Our studies have investigated coronary endothelial f
unction after exposure to hyperkalaemia (K+ 20 or 50 mmol/L). Endothel
ium-dependent relaxation and hyperpolarization of the coronary smooth
muscle and intracellular free calcium concentration in the endothelial
cell were measured with regard to K+ exposure.3. Endothelium-derived
hyperpolarizing factor (EDHF)-mediated relaxation to A23187, bradykini
n, and substance P in the presence of either U46619 (10 nmol/L)- or K (25 mmol/L)-induced contraction was reduced after exposure to either
20 or 50 mmol/L K+. 4. The hyperpolarization of the membrane potential
in response to the endothelium-derived relaxing factor (EDRF) stimuli
was also reduced by exposure to K+.5. The intracellular free calcium
concentration remained unchanged after exposure to hyperkalaemia. 6. W
e conclude that the EDHF-mediated coronary endothelial function is imp
aired after exposure to hyperkalaemic cardioplegia. The impairment of
this function is due to the changed effect of EDHF on the smooth muscl
e cell, probably through partially depolarizing the membrane and affec
ting K+ channels rather than alteration of its biosynthesis/release in
the endothelial cell. It may be of use to search for a new cardiopleg
ia that preserves this endothelial function during open heart surgery.